Neeb L, Reuter U
Charité Campus Mitte, Universitätsmedizin Berlin, Department of Neurology, Charitéplatz 1, 10117, Berlin, Germany.
CNS Neurol Disord Drug Targets. 2007 Aug;6(4):258-64. doi: 10.2174/187152707781387233.
The potent vasodilatator and messenger molecule nitric oxide (NO) is believed to play a key role in migraine pathogenesis. NO donors such as glyceryl trinitrate (GTN) can cause headache. Infusion of GTN leads to a migraine attack in migraineurs with a latency of 4 to 6 hours. In this review we focus in the role of nitric oxide and the transcription factor nuclear factor-kappaB (NF-kappaB) in migraine pathophysiology in humans and animal models. NO is involved in pain transmission, hyperalgesia, chronic pain, inflammation and central sensitization mostly in a cyclic guanosinemono-phosphate (cGMP) dependent way. We aim to illustrate how NO is implicated in the induction of a migraine attack in migraineurs and how experimental animal models may help to elucidate the mechanisms of the human GTN response. Because of the role of NO in migraine we try to assess if and how the action of preventative migraine drugs involves the NO pathways. More knowledge about the involvement of NO in the genesis of migraine headache may also provide possible future therapeutic targets for acute migraine therapy.
强效血管扩张剂及信使分子一氧化氮（NO）被认为在偏头痛发病机制中起关键作用。硝酸甘油（GTN）等NO供体可引发头痛。对偏头痛患者输注GTN会在4至6小时的潜伏期后引发偏头痛发作。在本综述中，我们聚焦于一氧化氮和转录因子核因子-κB（NF-κB）在人类和动物模型偏头痛病理生理学中的作用。NO大多通过环磷酸鸟苷（cGMP）依赖性方式参与疼痛传递、痛觉过敏、慢性疼痛、炎症及中枢敏化。我们旨在阐明NO如何在偏头痛患者中引发偏头痛发作，以及实验动物模型如何有助于阐明人类对GTN反应的机制。鉴于NO在偏头痛中的作用，我们试图评估预防性偏头痛药物的作用是否以及如何涉及NO途径。更多关于NO参与偏头痛性头痛发生的知识也可能为急性偏头痛治疗提供未来可能的治疗靶点。
